The remaining 60% of risk is attributable to a combination of other potential modifiable factors (e.g., sleep and hypercholesterolemia) and non-modifiable factors, such as a genetic predisposition (e.g., the Apolipoprotein E ε4 genotype (APOE4) is estimated to account for 7% of the attributable risk). This evidence concerns the gene APOE and Hypercholesterolemia.